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Biomedical subjects

S Ying

Publications and source records attributed to S Ying.

At least 55 records · Page 3Linked to original sources
PubMed1997

Effects of rapamycin, cyclosporin A, and dexamethasone on interleukin 5-induced eosinophil degranulation and prolonged survival.

Interleukin-5 (IL-5) enhances eosinophil degranulation and prolongs eosinophil survival. Rapamycin, cyclosporin A, and dexamethasone have been shown to influence either cytokine transcription, cytokine-mediated signalling, or degranulation by granulocytes. The study aimed to determine whether these agents inhibited IL-5-enhanced eosinophil survival or degranulation. Peripheral blood eosinophils were isolated from atopic subjects. The effects of serial dilutions (10(-6)-10(-9) M) of these drugs or vehicle control on 1) the viability of eosinophils cultured (1-5 days) in the presence and absence of recombinant human IL-5, as measured by propidium iodide staining and flow cytometry, and 2) degranulation of eosinophils preincubated (45 min) with rhIL-5 or medium control, as measured by eosinophil cationic protein (ECP) release after stimulation with serum-coated Sephadex beads, were assessed. Dexamethasone and rapamycin produced significant, concentration-dependent inhibition of IL-5-enhanced eosinophil survival at pharmacologic concentrations, whereas cyclosporin A did not. Prior incubation of eosinophils with IL-5, as compared with medium control, significantly enhanced ECP release by eosinophils on subsequent exposure to serum-coated Sephadex beads. Cyclosporin A and rapamycin significantly inhibited IL-5-enhanced ECP release in a concentration-dependent fashion, whereas dexamethasone did not. All three drugs had no significant effect on eosinophil survival and degranulation in the absence of IL-5. Our results suggest that immunosuppressive drugs may inhibit IL-5-mediated mechanisms in eosinophils which result in enhanced survival and release of granule contents. These findings may be relevant to the further development of therapeutic strategies in allergic diseases.

Anti-Inflammatory Agents↗
PubMed1997

The GM-CSF analogue E21R induces apoptosis of normal and activated eosinophils.

There is evidence that eosinophils have an important role in the pathogenesis of allergy and asthma. These cells are regulated by two classes of polypeptides, the colony-stimulating factors, such as granulocyte-macrophage colony-stimulating factor (GM-CSF), and the chemokines, such as RANTES and eotaxin. GM-CSF is involved in the production, survival, and functional activation of eosinophils. RANTES and eotaxin regulate the migration of eosinophils to inflammatory sites, but any effect of these chemokines on eosinophil survival is not known. In this study we demonstrate that although GM-CSF promoted eosinophil survival, the specific GM-CSF analogue E21R induced apoptosis of eosinophils. Apoptosis was observed with unstimulated as well as with chemokine (RANTES and eotaxin)-activated eosinophils. Neither RANTES nor eotaxin supported eosinophil survival, and a RANTES antagonist did not affect either cell survival or apoptosis. E21R also induced apoptosis of eosinophils from asthmatic patients. These findings suggest that the GM-CSF receptor may actively control the death as well as the survival of eosinophils, and thus precisely regulate their numbers and activities. Our data also indicate that chemokines are not involved in regulating the lifespan of eosinophils. The introduction of the GM-CSF analogue E21R may offer a novel therapy in inflammatory diseases associated with eosinophil infiltration of different etiologies.

Apoptosis↗
PubMed1997

Bronchial mucosal expression of the genes encoding chemokines RANTES and MCP-3 in symptomatic atopic and nonatopic asthmatics: relationship to the eosinophil-active cytokines interleukin (IL)-5, granulocyte macrophage-colony-stimulating factor, and IL-3.

Intrinsic (nonatopic) asthma is considered to be a distinct pathogenetic variant of asthma since, unlike extrinsic (atopic) asthma, patients are skin-prick test negative to common aeroallergens and have total serum immunoglobulin E concentrations within the normal range. However both atopic and nonatopic asthma are characterized by chronic inflammation of the bronchial mucosa in which eosinophils are prominent and are believed to be associated with local tissue damage. Therefore, specific eosinophil chemoattractants acting in concert with factors which prolong eosinophil survival may at least partly account for selective eosinophil recruitment to the asthmatic bronchial mucosa. The CC chemokines RANTES and monocyte chemotactic protein 3 (MCP-3) are potent eosinophil chemotactic factors, while the cytokines interleukin (IL)-5, granulocyte macrophage-colony-stimulating factor (GM-CSF), and IL-3 prolong eosinophil survival. We have tested the hypothesis that elevated numbers of cells expressing mRNA for RANTES and MCP-3, as well as IL-5, GM-CSF, and IL-3 are present in bronchial biopsies from atopic and nonatopic asthmatics compared with atopic and nonatopic nonasthmatic controls. The technique of in situ hybridization using 35S-labeled riboprobes was employed to detect mRNA+ bronchial mucosal cells. Compared with controls we observed significant increases in the numbers of cells expressing RANTES and MCP-3, as well as IL-5, GM-CSF, and IL-3 (all P values < 0.001) in atopic and nonatopic asthmatics. These observations support the view that atopic and nonatopic asthma are associated with combined bronchial mucosal expression of CC chemokines (RANTES and MCP-3), together with eosinophil-active cytokines (IL-5, GM-CSF, and IL-3). These cytokines might contribute to the bronchial mucosal accumulation of activated eosinophils in both atopic and nonatopic variants of asthma.

Asthma↗
PubMed1997

Association of apoptosis of neutrophils and eosinophils and their ingestion by macrophages with resolution of the allergen-induced cutaneous late-phase response in atopic human subjects.

The allergen-induced cutaneous late-phase response serves as a model of allergic inflammation and is associated with infiltration of neutrophils, eosinophils, T cells, and macrophages. The mechanisms controlling the resolution of allergic inflammatory processes and the fate of infiltrating cells are uncertain. We observed that both the magnitude of the late-phase response and the numbers of infiltrating neutrophils and eosinophils peaked at 6 hr, persisted for 48 hr, but resolved completely by 7 days. In contrast, T-cell and macrophage numbers peaked between 24 and 72 hr after allergen challenge and persisted for up to 7 days. By using the techniques of terminal deoxynucleotidyl transferase-mediated biotin-deoxyuridine 5'-triphosphate (dUTP) nickend-labeling (TUNEL) and by combining TUNEL with immunohistochemistry, we tested the hypothesis that the resolution of the late-phase response is associated with apoptosis of neutrophils and eosinophils, with subsequent engulfment of apoptotic cells and apoptotic bodies by tissue macrophages. As the cutaneous late-phase response resolved, there was a progressive increase (peaking at 72 hr) in the total numbers of TUNEL-positive (TUNEL+) cells and in the numbers of macrophages that had engulfed apoptotic cells and bodies. The majority of TUNEL+ cells were identified as neutrophils and eosinophils. In contrast, very little apoptosis was associated with T cells or macrophages. These experiments represent a novel demonstration of cell type-specific apoptosis in vivo in human allergic inflammatory tissue and suggest that phagocytosis by macrophages of apoptotic neutrophils and eosinophils may be a mechanism that regulates resolution of the atopic allergic inflammatory response.

Adolescent↗
PubMed1996

Human eosinophils express messenger RNA encoding RANTES and store and release biologically active RANTES protein.

Eosinophils synthesize and store various cytokines with potential autocrine activity. We hypothesized that eosinophils synthesize and store RANTES, a CC-chemokine with potent eosinophil chemotactic activity. Expression of RANTES mRNA in highly purified eosinophil populations was detected by reverse transcription followed by polymerase chain reaction analysis. In situ hybridization (ISH) with 35S-labeled RANTES-specific riboprobes showed that 6.8-10% of peripheral blood eosinophils obtained from atopic subjects expressed RANTES mRNA, increasing to 25% after incubation (16 h) with interferon (IFN)-gamma, but not ionomycin in vitro. Peripheral blood eosinophils also showed specific immunoreactivity with an anti-RANTES monoclonal antibody, consistent with translation of the mRNA. By enzyme-linked immunosorbent assay, blood eosinophils were shown to contain a median of 7300 pg (range 5200-8800) RANTES per 10(6) cells, of which a mean of 24% was released into culture supernatants after stimulation of the cells with serum-coated particles in vitro. These culture supernatants exhibited eosinophil chemotactic activity which was inhibited (mean 68%) by a specific anti-RANTES antibody. Sequential immunocytochemistry and ISH on biopsies obtained from allergen-induced late-phase cutaneous reactions showed that 55-75% of the infiltrating RANTES mRNA+ cells were EG2+ eosinophils. Allergen, but not diluent challenge, was also associated with a time-dependent increase in the number of cells showing RANTES immunoreactivity. Of these cells, 55% were identified as eosinophils by morphological criteria. Thus, human eosinophils have the capacity to synthesize, store and secrete physiologically relevant quantities of RANTES, and may therefore be an important source of this chemokine in allergic inflammation.

Allergens↗
PubMed1996

Grass pollen immunotherapy inhibits allergen-induced infiltration of CD4+ T lymphocytes and eosinophils in the nasal mucosa and increases the number of cells expressing messenger RNA for interferon-gamma.

BACKGROUND: Grass pollen injection immunotherapy is effective in patients with summer hay fever, although efficacy must be balanced against possible side effects. The mechanism of immunotherapy is unknown but may be related to its ability to inhibit allergen-induced late responses, which are known to be characterized by infiltration of T lymphocytes, eosinophils, and cells with messenger RNA for so-called TH2-type cytokines (IL-4 and IL-5). OBJECTIVE: This study was designed to observe the effect of grass pollen immunotherapy on late nasal responses and associated cellular infiltration and cytokine mRNA expression. METHODS: We performed local nasal provocation with grass pollen (and a control challenge) in 28 patients after a 12-month double-blind, placebo-controlled trial of immunotherapy. Nasal biopsy specimens were obtained at 24 hours and processed for immunohistology and in situ hybridization studies. RESULTS: Grass pollen immunotherapy inhibited allergen-induced immediate (0 to 60 minutes) increases in sneezing (p < 0.02) and nasal blocking (p < 0.01) and late (0 to 24 hours) nasal symptoms (p < 0.05). Immunotherapy also inhibited the associated infiltration of the nasal mucosa by CD4+ T lymphocytes and total (major basic protein-containing) and "activated" (cationic protein-secreting) eosinophils (all p = 0.03). There was a significant (p = 0.04) increase in cells expressing mRNA for interferon-gamma at 24 hours after allergen challenge, which correlated inversely with patients' seasonal symptoms (r = -0.65, p < 0.05) and medication requirements (r = -0.75, p < 0.02) during the pollen season. CONCLUSION: The results suggest that successful grass pollen immunotherapy for summer hay fever may act by inhibiting allergen-induced T lymphocyte and eosinophil recruitment and eosinophil activation in the target organ, possibly through a mechanism involving protective local increases in TH1-type cells.

Adult↗
PubMed1996

Effect of cetirizine and prednisolone on cellular infiltration and cytokine mRNA expression during allergen-induced late cutaneous responses.

BACKGROUND: The ability of cetirizine to inhibit eosinophil infiltration into the sites of allergen-induced cutaneous late-phase reactions is controversial. A previous skin biopsy study gave negative results with 15 mg of cetirizine as a single dose. OBJECTIVE: To confirm these findings we have used cetirizine (30 mg daily) for 5 days and compared the results with prednisolone (20 mg daily for 5 days) as a positive control. The effect of these agents on mRNA positive cells for interleukin-3 (IL-3), interleukin-4, interleukin-5 and granulocyte/macrophage-colony stimulating factor (GM-CSF) was also evaluated. METHODS: A double-blind, placebo-controlled cross-over study (n = 12) was followed. After each treatment 30 biological units (BUs) of Dermatophagoides pteronyssinus or Phleum pratense were injected intradermally and the early (15 min) and late-phase response sizes (6 and 24 h) were measured. Skin biopsies were taken at 24 h for immunocytochemistry and in situ hybridization. RESULTS: Cetirizine but not prednisolone inhibited the early-phase response (37%, P = 0.004). In contrast prednisolone, but not cetirizine, significantly inhibited the size of the late-phase reaction at 24 h (70%, P = 0.021). This was associated with significant decreases in total (MBP+) and activated (EG2+) eosinophils (P = 0.019 and 0.014, respectively), as compared with placebo. There were also clear but non-significant reductions in interleukin-3, interleukin-4, interleukin-5 and granulocyte/macrophage-colony stimulating factor mRNA+ cells. CONCLUSION: Prednisolone, but not cetirizine, inhibited both the magnitude of the allergen-induced late-phase response and the accompanying local eosinophil infiltration. These corticosteroid effects were associated with a reduction in cells expressing mRNA for 'TH2-type' cytokines.

Adult↗
PubMed1996

High-affinity IgE receptor (FcepsilonRI)-bearing cells in bronchial biopsies from atopic and nonatopic asthma.

Asthma is characterized by bronchial mucosal inflammation. Although allergen-induced activation of cells binding allergen-specific immunoglobulin E (IgE) through high-affinity receptors (Fc(epsilon)RI) is believed to play some role in asthma, inappropriate synthesis of total or allergen-specific IgE cannot be demonstrated in some ("intrinsic") patients despite the fact that the nature of the bronchial inflammation is similar to that in atopic ("extrinsic") asthmatics. We have studied the numbers and phenotype of Fc(epsilon)RI-bearing cells in bronchial biopsies from 12 atopic and 10 nonatopic asthmatic patients and compared our findings with 10 atopic and 12 nonatopic control subjects using single and double immunohistochemistry. Significantly increased numbers of Fc(epsilon)RI-bearing cells were identified in bronchial biopsies from atopic and nonatopic asthmatics and atopic control subjects when compared with normal controls (p = 0.001, 0.006, and 0.0006, respectively). In asthmatics and atopics the majority of Fc(epsilon)RI-bearing cells were identified as mast cells and macrophages; a much smaller percentage were eosinophils. We conclude that elevated numbers of high-affinity IgE receptor-bearing cells are a feature of bronchial biopsies of asthmatic subjects, irrespective of their atopic status.

Adult↗
PubMed1996

IL-4 and IL-5 mRNA and protein in bronchial biopsies from patients with atopic and nonatopic asthma: evidence against "intrinsic" asthma being a distinct immunopathologic entity.

Intrinsic (nonatopic) asthma is considered to be a distinct pathogenetic variant of asthma since, unlike extrinsic (atopic) asthma, patients with the disease are skin test-negative to common aeroallergens, and have total serum IgE concentrations within the normal range. Nevertheless, the recent demonstration of increased numbers of cells expressing the high-affinity IgE receptor in bronchial biopsies from atopic and nonatopic asthmatic subjects, together with epidemiologic evidence indicating that serum IgE concentrations relate closely to asthma prevalence regardless of atopic status, suggests that IgE-mediated mechanisms may participate in the pathogenesis of both atopic and nonatopic asthma. Furthermore both variants of the disease are associated with bronchial mucosal eosinophilic inflammation. Interleukin-4 (IL-4) is an essential cofactor for IgE synthesis, and there is strong evidence that IL-5 plays a major role in eosinophil accumulation in asthmatic inflammation. For these reasons we compared the expression of IL-4 and IL-5 mRNA and protein product using a semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) amplification, in situ hybridization, and immunohistochemistry in bronchial biopsies from symptomatic atopic and nonatopic asthmatic subjects and atopic and nonatopic controls. The results showed that as compared with controls, biopsies from both groups of asthmatic subjects had increased numbers of IL-4 and IL-5 mRNA copies relative to beta-actin mRNA as detected by RT-PCR. Similarly, in situ hybridization and immunohistochemistry demonstrated increased numbers of cells expressing IL-4 and IL-5 mRNA and protein in asthmatic subjects, irrespective of their atopic status. We conclude that individuals with either atopic or nonatopic asthma show infiltration of the bronchial mucosa with cells expressing Th2-type cytokines, providing further evidence for similarities in the immunopathogenesis of these clinically distinct forms of asthma.

Adult↗
PubMed1996

Identification of interleukin-2 in human peripheral blood eosinophils.

Interleukin-2 (IL-2) is an essential growth factor for T cells. Previous studies have shown that human peripheral eosinophils respond to IL-2 in chemotaxis and express the IL-2 receptor (CD25). In addition, eosinophils have been shown to transcribe messenger RNA for IL-2. The aim of the present study was to determine whether eosinophils translate mRNA for IL-2 and to determine the site of intracellular localization. By immunocytochemistry, an average of 9% of cells showed cytoplasmic staining for IL-2 in freshly isolated unstimulated blood eosinophils obtained from asthmatic subjects who were not receiving oral corticosteroid treatment (n = 5). Freshly isolated, disrupted, highly purified eosinophils (> 99%, by CD16- immunomagnetic selection) contained an average of 6 pg/10(6) cells of IL-2 measured by a specific enzyme linked immunosorbent assay (ELISA) (n = 7). Purified eosinophil incubated with serum-coated Sephadex beads showed an increase in the amount of intracellularly-retained IL-2 (26.2 +/- 7.2 pg/10(6) cells) with some evidence for release of this cytokine but only in three out of six eosinophil preparations (range 1.3-5.8 pg/10(6) cells). The intracellular localization of IL-2 was determined by fractionation of the cells on a linear (0-45%) Nycodenz gradient in sucrose buffer followed by detection of IL-2 in the fractions using an IL-2-specific ELISA and dot blotting. The majority of the IL-2 detected co-eluted with known eosinophil granule markers (i.e. major basic protein (MBP), eosinophil cationic protein (ECP), eosinophil peroxidase (EPO) and beta-hexosaminidase) but small quantities were also detected in the cytosolic (lactate dehydrogenase-(LDH) associated) and membrane (CD9+) fractions. Immunogold labelling of intact eosinophils using an anti-IL-2 monoclonal antibody confirmed IL-2 immunoreactivity in association with the eosinophil crystalline granule cores. These data are consistent with the hypothesis that eosinophils synthesize, release and store IL-2 largely within cystalloid granules. This stored IL-2 may serve as a reservoir for rapid release of IL-2 in inflammatory reactions associated with eosinophilia.

Asthma↗
PubMed1995

Identification of messenger RNA for IL-4 in human eosinophils with granule localization and release of the translated product.

Human eosinophils are cytokine-producing cells that are prominent in IgE-dependent allergic tissue reactions. IL-4 promotes the development of the Th2-type phenotype in T cells and is an essential cofactor for IgE production by B cells. We detected mRNA for IL-4 by reverse transcription-PCR in blood eosinophils from atopic asthmatics. By specific ELISA, 108 +/- 20 pg of IL-4 protein/10(6) cells could be extracted from whole cells, and approximately 30% of the IL-4 was released after incubation with serum-coated particles. Using immunocytochemistry, eosinophils from atopic asthmatics and nonatopic controls showed IL-4 immunoreactivity using an anti-IL-4 mAb. IL-4 was located predominantly in the eosinophil granules, as shown by both immunogold electron microscopy and a cell fractionation technique that dissociated cell granules from membrane and cytosolic components. IL-4 mRNA colocalized with eosinophils (using sequential immunocytochemistry with an eosinophil-specific (EG2) mAb and in situ hybridization using an IL-4-specific antisense riboprobe) in both cell cytospins from bronchoalveolar lavage fluid from asthmatics as well as skin biopsies obtained from allergen-induced late phase (6-h) reactions in atopic subjects. Using double immunocytochemistry on skin biopsies with eosinophil- and IL-4-specific mAb, 83.5 +/- 3.5% of eosinophils were IL-4+. Conversely, eosinophils accounted for 46.5 +/- 3.9% of the total cells expressing IL-4 immunoreactivity. Thus, human eosinophils express mRNA for IL-4, and the translated product is contained within the crystalloid granule from which it is released after stimulation with serum-coated particles. These observations are consistent with the hypothesis that eosinophils contribute to the development of the Th2 phenotype by T cells infiltrating atopic allergic reactions as well as to IgE synthesis.

Asthma↗
PubMed1995

The kinetics of allergen-induced transcription of messenger RNA for monocyte chemotactic protein-3 and RANTES in the skin of human atopic subjects: relationship to eosinophil, T cell, and macrophage recruitment.

The C-C chemokines RANTES and monocyte chemotactic protein-3 (MCP-3) are potent chemoattractants in vitro for eosinophils and other cell types associated with allergic reactions. We tested the hypothesis that the allergen-induced infiltration of eosinophils, T cells, and macrophages in the skin of atopic subjects is accompanied by the appearance of mRNA+ cells for RANTES and MCP-3. Cryostat sections were obtained from skin biopsies from six subjects 6, 24, and 48 h after allergen challenge. Tissue was processed for immunocytochemistry (ICC) and for in situ hybridization using 35S-labeled riboprobes for RANTES and MCP-3. In contrast to diluent controls, allergen provoked a significant increase in mRNA+ cells for MCP-3, which peaked at 6 h and progressively declined at 24 and 48 h. This paralleled the kinetics of total (major basic protein positive [MBP]+) and activated (cleaved form of eosinophil cationic protein [EG2]+) eosinophil infiltration. The allergen-induced expression of cells mRNA+ for RANTES was also clearly demonstrable at 6 h. However, the numbers were maximal at 24 h and declined slightly at the 48-h time point. The number of mRNA+ cells for RANTES paralleled the kinetics of infiltration of CD3+, CD4+, and CD8+ T cells whereas the number of CD68+ macrophages was still increasing at 48 h. These data support the view that MCP-3 is involved in the regulation of the early eosinophil response to specific allergen, whereas RANTES may have more relevance to the later accumulation of T cells and macrophages.

Adult↗
PubMed1995

Dysregulation of interleukin 4, interleukin 5, and interferon gamma gene expression in steroid-resistant asthma.

In steroid-resistant (SR) asthma, there is a lack of clinical responsiveness to oral prednisone. Previous studies indicate that this may be explained by the effect of the combination of interleukin 2 (IL-2) and IL-4 on glucocorticoid receptor binding affinity. By contrast, steroid-sensitive (SS) asthmatics respond well to glucocorticoids, and this is accompanied by a decrease in the numbers of bronchoalveolar lavage (BAL) messenger RNA+ (mRNA+) cells expressing IL-4 and IL-5, and an increase in interferon gamma (IFN-gamma) transcripts. In the present study, we hypothesized that SR asthma is associated with alterations in T helper types 1/2 (Th2/Th1)-type cytokine gene expression. BAL was performed in six SR asthmatics and six SS asthmatics, before and after a 1-wk course of 40 mg daily prednisone. mRNA+ cells for IL-2, IL-4, IL-5, and IFN-gamma was measured by in situ hybridization using 35S-labeled RNA probes. Before prednisone therapy, there were significantly greater numbers of BAL cells (per 1,000) expressing IL-2 mRNA (p < 0.01) and IL-4 mRNA (p < 0.05) in SR asthmatics as compared with SS asthmatics, but no differences between the two groups in the numbers of BAL cells expressing IFN-gamma or IL-5 mRNA expression were observed. After a 1-wk course of prednisone, IL-2 expression was not altered in either group. However, SS asthmatics had a significant decrease in the numbers of BAL cells expressing mRNA for IL-4 (p < 0.01) and IL-5 (p < 0.001), and a rise in the numbers of IFN-gamma mRNA+ cells (p < 0.01). In contrast, after prednisone treatment, SR asthmatics had no significant change in either the number of BAL cells expressing mRNA for IL-4 or IL-5. Of note, there was an unexpected decrease in the numbers of IFN-gamma mRNA+ cells (p = 0.05). Our current findings indicate that SR asthma is associated with a dysregulation of the expression of the genes encoding for Th2/Th1 cytokines in airway cells and is compatible with the concept that a combination of IL-2 and IL-4 induce glucocorticoid (GR) binding affinity and T cell responsiveness to glucocorticoids.

Adult↗
PubMed1995

Phenotype of cells expressing mRNA for TH2-type (interleukin 4 and interleukin 5) and TH1-type (interleukin 2 and interferon gamma) cytokines in bronchoalveolar lavage and bronchial biopsies from atopic asthmatic and normal control subjects.

We investigated the phenotype of cells expressing messenger RNA encoding interleukin 4 (IL-4), IL-5, IL-2, and interferon gamma (IFN-gamma) in bronchoalveolar lavage (BAL) and bronchial biopsies (BX) from seven mild atopic asthmatic patients and nine nonasthmatic controls. Immunocytochemistry followed by in situ hybridization using either 35S- or digoxigenin-labeled riboprobes was performed on cytospins from BAL and BX, respectively. With BAL or BX, in situ hybridization alone showed significant increases in percentages of IL-2, IL-4, and IL-5 mRNA+ cells when asthmatics were compared to nonasthmatic controls. Double immunocytochemistry-in situ hybridization revealed that > 70% of IL-4 and IL-5 mRNA+ cells were activated T cells (CD3+). The remaining IL-4 and IL-5 mRNA+ signals were colocalized to tryptase+ mast cells, and activated eosinophils (EG2+). Rare IL-4 and IL-5 mRNA+ cells were observed in nonasthmatic controls, the majority being CD3+ cells, as were IL-2 and IFN-gamma mRNA+ cells (in both asthmatics and controls). A few IL-4 (< 8%) and IL-5 (< 5%) mRNA+ signals did not colocalize with any of the cells identified by immunocytochemistry. Thus, we provide further evidence that CD3+ T cells are the most abundant cells expressing IL-4 and IL-5 mRNA in BAL and BX from allergic asthma. Fewer, but detectable, numbers of tryptase+ mast cells and EG2+ eosinophils also expressed these transcripts.

Adult↗
PubMed1994

Evidence for a Th1-like bronchoalveolar T-cell subset and predominance of interferon-gamma gene activation in pulmonary tuberculosis.

Mycobacterium-specific human helper T-cell clones produce a Th1 pattern of cytokines in vitro: interferon-gamma (IFN-gamma) and interleukin-2 (IL-2), but little or no IL-4 or IL-5. To test the hypothesis that a similar Th1-like pattern of cytokine gene expression occurs in vivo in pulmonary tuberculosis we used in situ hybridization to detect cytokine mRNA expression by bronchoalveolar lavage cells from nine patients with microbiologically confirmed tuberculosis and nine control subjects. Because IFN-gamma may also originate from alveolar macrophages, simultaneous immunocytochemistry and in situ hybridization was applied to determine whether cytokine mRNA was localized to bronchoalveolar macrophages in addition to T-lymphocytes. When samples from patients with tuberculosis and control subjects were compared, there was a significant increase in numbers of IFN-gamma mRNA-positive BAL cells per 1,000 among patients with tuberculosis (p < 0.01). Differences between the two groups in the proportions of cells expressing IL-2, IL-4, or IL-5 mRNA were not significant. Expression of IFN-gamma mRNA by macrophages was detected (median, 14.3% of IFN-gamma mRNA-positive BAL cells). However, the majority of IFN-gamma mRNA expressing BAL cells were T-lymphocytes (median, 80.7%). Activation of Th1-like bronchoalveolar T-lymphocytes, together with production of IFN-gamma by alveolar macrophages, may contribute to the local cellular immune response in pulmonary tuberculosis.

Adolescent↗
PubMed1994

[Effects of electro-acupuncture on EEG during transient global ischemia and reperfusion in gerbils].

In the model of gerbil of acute global ischemia and reperfusion, we studied the effects of electro-acupuncture (EA) on total power of EEG at different periods of global ischemia and reperfusion. The "Fengfu" (GV 16) and "Jinsuo" (GV 8) points were stimulated by electrical pulse with frequency 7 Hz and intensity of 5-6 mA for 30 min. Recording was made before ischemia and 0 min, 15 min, 30 min, 60 min, 120 min and 240 min after reperfusion respectively. The results were as follows: 1. In the control group, after 10 min of ischemia, the amplitude of EEG was severely inhibited, even became flatten, and the total power of EEG was significantly decreased to 1.41 + 1.29%. After reperfusion, the recovery of total power was very slow. The peak level of recovery occurred at 120 min following reperfusion was 27.39 + 11.31%. 2. In comparison with the control group, the EA remarkably improved the recovery of EEG after ischemia and reperfusion. The recovery of total power was 71.45 + 16.46% (P < 0.01), and 75.27 + 18.43% (P < 0.01) at 120 min and 240 min after reperfusion respectively. These results strongly indicate that EA could reduce the EEG inhibition during global ischemia and improve the recovery after reperfusion.

Animals↗